Abdominal Pain

  1. History
  2. Physical Examination
  3. Diagnostic evaluation
    1. Anatomy
  4. Differential Diagnoses of Abdominal Pain by Location
  5. Classification by acuity
    1. Acute emergencies
      1. Evaluation of acute abdominal pain
    2. Evaluation of chronic abdominal pain
    3. Specific comorbidities

History


  • R/O catastrophic emergencies like AAA rupture
  • Acute emergency vs acute non-emergent vs chronic
  • Description
    • Onset, progression, modulation
    • Quality
    • Location
  • Associated symptoms
  • ROS especially GI/GU
  • PMH
  • PSH
  • Medications and allergies
  • Comorbidities and Special populations – HIV, Pregnant, elderly, Sickle cell

Physical Examination


  • Vitals
  • Inspection
  • Auscultation
  • Palpation
  • Percussion
  • Rectal
  • Pelvic

Diagnostic evaluation


Anatomy

Differential Diagnoses of Abdominal Pain by Location

Right Upper Quadrant

Epigastric

Left Upper Quadrant

Cholecystitis

Cholangitis

Pancreatitis

Pneumonia/empyema

Pleurisy/pleurodynia

Subdiaphragmatic abscess

Hepatitis

Budd-Chiari syndrome

Peptic ulcer disease

Gastritis

GERD

Pancreatitis

Myocardial infarction

Pericarditis

Ruptured aortic aneurysm

Esophagitis

Splenic infarct

Splenic rupture

Splenic abscess

Gastritis

Gastric ulcer

Pancreatitis

Subdiaphragmatic abscess

Right Lower Quadrant

Periumbilical

Left Lower Quadrant

Appendicitis

Salpingitis

Inguinal hernia

Ectopic pregnancy

Nephrolithiasis

Inflammatory bowel disease

Mesenteric lymphadenitis

Typhlitis

Early appendicitis

Gastroenteritis

Bowel obstruction

Ruptured aortic aneurysm

Diverticulitis

Salpingitis

Inguinal hernia

Ectopic pregnancy

Nephrolithiasis

Irritable bowel syndrome

Inflammatory bowel disease

Diffuse Nonlocalized Pain

Gastroenteritis

Mesenteric ischemia

Bowel obstruction

Irritable bowel syndrome

Peritonitis

Diabetes

Malaria

Familial Mediterranean fever

Metabolic diseases

Psychiatric disease

from Harrisons IM

Classification by acuity


Acute emergencies

Patients in whom there are concerns for life-threatening causes of abdominal pain should be referred to the emergency department.

These include those with:

  • Unstable vital signs
  • Signs of peritonitis on the abdominal exam (eg, abdominal rigidity, rebound tenderness, and/or pain that worsens when the examiner lightly bumps the stretcher)
  • Concern that the abdominal pain is from a life-threatening condition (eg, acute bowel obstruction, acute mesenteric ischemia, perforation, acute myocardial infarction, ectopic pregnancy)
Evaluation of acute abdominal pain
  • See DD according to location
  • Diffuse?
  • Further evaluation will depend on the results from the initial evaluation. As examples:
    • Patients with a history concerning for IBD with extraintestinal manifestations and/or family history should be evaluated as appropriate. (See UptoDate)
    • The combination of metabolic acidosis and elevated blood glucose strongly suggests diabetic ketoacidosis (DKA) as the etiology of the symptoms. It is important to keep in mind that an intraabdominal infection could precipitate DKA in a patient with diabetes. (See UptoDate)
    • Patients with hyponatremia or hyperkalemia and symptoms of fatigue, malaise, nausea and vomiting, and symptoms of hypotension may have adrenal insufficiency. (See UptoDate)
    • Hypercalcemia can cause abdominal pain, either directly or as an etiology for pancreatitis or constipation.

Evaluation of chronic abdominal pain

  • Initial work up
    • CBC
    • CMP
    • Amylase and lipase
    • Iron Studies
    • Anti-tissue transglutaminase
  • Subsequent work-up
    • < 50 IBS? Or more work up
    • > 50 need further workup including imaging due to the age factor
    • Less common causes of abdominal pain (table in Uptodate) should be considered in patients with repeated visits for the same complaint without a definite diagnosis, in an ill-appearing patient with minimal or nonspecific findings, in patients with pain out of proportion to clinical findings, and in immunocompromised patients. Examples of such cases include:
      • Right upper quadrant pain after cholecystectomy mimics biliary colic and could be functional biliary pain; it could also arise from the intermittent passage of stones that have formed in the bile ducts, the passage of sludge, or the sphincter of Oddi dysfunction.
      • Chronic, partial small bowel obstruction may occur in some patients. Patients usually present with chronic postprandial abdominal discomfort and variable nausea. Abdominal distention and tympany may be present, but usually without any fluid or electrolyte derangements. (See Uptodate)
      • Very rare causes of intermittent acute severe abdominal pain should be considered in the setting of a positive family history (eg, familial Mediterranean fever, hereditary angioedema, acute intermittent porphyria [AIP]); in the case of AIP, the diagnosis may be considered even without a family history of the disease.

Specific comorbidities

  • Pregnancy
  • Elderly
  • HIV
  • SCD

Headache

Classification

Common Causes of Headache

PRIMARY HEADACHE

SECONDARY HEADACHE

TYPE

%

TYPE

%

Tension-type

69

Systemic infection

63

Migraine

16

Head injury

4

Idiopathic stabbing

2

Vascular disorders

1

Exertional

1

Subarachnoid hemorrhage

<1

Cluster

0.1

Brain tumor

0.1

Source: After J Olesen et al: The Headaches. Philadelphia, Lippincott Williams & Wilkins, 2005

Anatomy

The key structures involved in primary headaches are the following:

  • The large intracranial vessels and dura mater, and the peripheral terminals of the trigeminal nerve that innervate these structures
  • The caudal portion of the trigeminal nucleus, which extends into the dorsal horns of the upper cervical spinal cord and receives input from the first and second cervical nerve roots (the trigeminocervical complex)
  • Rostral pain-processing regions, such as the ventroposteromedial thalamus and the cortex
  • The pain-modulatory systems in the brain that modulate input from the trigeminal nociceptors at all levels of the pain-processing pathways and influence vegetative functions, such as the hypothalamus and brainstem

From Netter

From Netter

Primary Headache evaluation

Classification of Daily or Near-Daily Headache

Primary

>4 H DAILY

<4 H DAILY

SECONDARY

Chronic migraine (a)

Chronic cluster headache (b

)

Posttraumatic

 Head injury

 Iatrogenic

 Postinfectious

Hemicrania continua

Chronic paroxysmal hemicrania

Inflammatory, such as

 Giant cell arteritis

 Sarcoidosis

 Behçet’s syndrome

Hemicrania continua (a)

SUNCT/SUNA

Chronic CNS infection

New daily persistent headache (a)

Hypnic headache

Medication-overuse headache (a)

From Harrisons IM

a May be complicated by medication overuse. b Some patients may have headaches>4 h/d.

Treatment of Primary Headaches

  • r/o emergency
  • r/o secondary headaches

Types

  • Chronic migraine
  • Chronic tension-type headache
  • Medication overuse headache
  • Hemicrania continua
  • New daily persistent headache (NDPH)

Chronic Migraine

Chronic Tension-type Headaches

Management of Medication Overuse: Outpatients

  • One approach is to reduce the medication dose by 10% every 1–2 weeks. Immediate cessation of analgesic use is possible for some patients, provided there is no contraindication. Both approaches are facilitated by the use of a medication diary maintained during the month or two before cessation; this helps to identify the scope of the problem. A small dose of a nonsteroidal anti-inflammatory drug (NSAID) such as naproxen, 500 mg bid, if tolerated, will help relieve residual pain as analgesic use is reduced. NSAID overuse is not usually a problem for patients with daily headaches when an NSAID with a longer half-life is taken once or twice daily; however, overuse problems may develop with shorter-acting NSAIDS. Once the patient has substantially reduced analgesic use, a preventive medication should be introduced.
  • Another widely used approach is to commence the preventive at the same time the analgesic reduction is started. It must be emphasized that preventives may not work in the presence of analgesic overuse, particularly with opioids. The most common cause of unresponsiveness to treatment is the use of a preventive when analgesics continue to be used regularly. For some patients, discontinuing analgesics is very difficult; often the best approach is to inform the patient that some degree of headache is inevitable during this initial period.

Management of Medication Overuse: Inpatients

  • Antiemetics and fluids;
  • clonidine is used for opioid withdrawal symptoms.
  • For acute intolerable pain during waking hours, aspirin, 1 g IV (not approved in the United States), is useful.
  • IM chlorpromazine can be helpful at night; patients must be adequately hydrated.
  • Three to five days into the admission, as the effect of the withdrawn substance wears off, a course of IV dihydroergotamine (DHE) can be used. DHE, administered every 8 h for 5 consecutive days, a treatment that is not stopped short if the headache settles, can induce a significant remission that allows a preventive treatment to be established. Serotonin 5-HT3 receptor antagonists, such as ondansetron or granisetron, or the neurokinin receptor antagonist, aprepitant, may be required with DHE to prevent significant nausea, and domperidone (not approved in the United States) orally or by suppository can be very helpful. Avoiding sedating or otherwise side effect–prone antiemetics is helpful.

Hemicrania Continua

New Chronic Daily Headaches

Edema

Edema evaluation

Attendance requirements:


Please see the “Guidelines” section.

Objectives:


  • Know the differential for this condition
  • Know how to approach a patient with this condition.
  • Know basic signs, symptoms, and treatment of other medical conditions in the differential.

Required reading:


  • Harrison’s chapter on Edema.
  • Also, review other “student slides” below. Know the differential and work-up algorithm!

Suggested reading:


Please use the text of your choice, e.g., UpToDate, Step-up to Medicine, Harrison’s, etc.

  • Pathophysiology of Edema

Student Slides: